Prevention of Oxidative Stress-Induced Retinal Pigment Epithelial Cell Death by the PPARgamma Agonists, 15-Deoxy-Delta 12, 14-Prostaglandin J(2).

Prevention of Oxidative Stress-Induced Retinal Pigment Epithelial Cell Death by the PPARgamma Agonists, 15-Deoxy-Delta 12, 14-Prostaglandin J(2).
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DOI:
10.1155/2008/720163
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发表时间:
2008
期刊:
影响因子:
2.9
通讯作者:
Bora NS
Bora NS
中科院分区:
医学3区
文献类型:
--
作者:
Chang JY;Bora PS;Bora NS

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细胞氧化应激在视网膜色素上皮(RPE)细胞老化死亡和年龄相关性黄斑变性的发展中起着重要作用。早期的报道表明,在视杆细胞吞噬视杆细胞外节的过程中,这些细胞中存在RPE氧化应激的增加和PPARγ mRNA的上调。这些研究表明,激活的过氧化物酶体增殖物激活受体γ可能调节细胞的氧化应激。本文简要回顾了最近的研究,调查在各种实验条件下的RPE氧化应激。本文就天然的PPARγ配体15 d-PGJ 2对RPE氧化应激的保护作用进行了综述。该试剂可上调谷胱甘肽并防止氧化剂诱导的细胞内活性氧簇积累、线粒体去极化和细胞凋亡。然而,这种药物的细胞保护作用不被其他PPARγ激动剂所共享。尽管如此,15 d-PGJ 2的这种性质可能有助于未来开发对抗氧化应激引起的视网膜疾病的药理学工具。
Cellular oxidative stress plays an important role in retinal pigment epithelial (RPE) cell death during aging and the development of age-related macular degeneration. Early reports indicate that during phagocytosis of rod outer segments, there is an increase of RPE oxidative stress and an upregulation of PPARγ mRNA in these cells. These studies suggest that activation of PPARγ may modulate cellular oxidative stress. This paper presents a brief review of recent studies that investigate RPE oxidative stress under various experimental conditions. This is followed by a detailed review on those reports that examine the protective effect of the natural PPARγ ligand, 15d-PGJ2, against RPE oxidative stress. This agent can upregulate glutathione and prevent oxidant-induced intracellular reactive oxygen species accumulation, mitochondrial depolarization, and apoptosis. The cytoprotective effect of this agent, however, is not shared by other PPARγ agonists. Nonetheless, this property of 15d-PGJ2 may be useful in future development of pharmacological tools against retinal diseases caused by oxidative stress.
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